1
Q
What is sinus arrhythmia?
A
Sinus arrhythmia is a physiological variation in heart rate that occurs with respiration, not a true rhythm abnormality.
2
Q
Does sinus arrhythmia indicate an abnormal heart rhythm
A
No. Despite its name, sinus arrhythmia is not a rhythm abnormality.
3
Q
What normally controls the heart rate in sinus rhythm?
A
The SA node, which depolarizes regularly at 60–100 beats per minute, moderated by sympathetic and parasympathetic nerves.
4
Q
How does respiration affect heart rate in sinus arrhythmia?
A
Heart rate increases during inspiration and decreases during expiration due to parasympathetic activity at the SA node.
5
Q
How is sinus arrhythmia detected on an ECG?
A
It manifests as varying R-R intervals, producing an irregular rhythm on the ECG
6
Q
Can sinus arrhythmia be exaggerated?
A
Yes, it may be more pronounced during deep or abnormal breathing.
7
Q
Is sinus arrhythmia considered pathological?
A
No, it is a normal physiological phenomenon and usually not associated with disease.
8
Q
What happens to parasympathetic activity during expiration?
A
Parasympathetic activity increases.
9
Q
How does increased parasympathetic activity affect the SA node?
A
The SA node paces slower, decreasing heart rate.
10
Q
What happens to the RR interval during expiration?
A
The RR interval becomes longer.
11
Q
How does inspiration affect parasympathetic activity?
A
Parasympathetic activity decreases during inspiration.
12
Q
What effect does decreased parasympathetic activity have on heart rate?
A
The SA node paces faster, increasing heart rate.
13
Q
How does the RR interval change during inspiration?
A
The RR interval becomes shorter.
14
Q
What are rhythms that do not originate in the SA node generally classified as?
A
They are either physiological ‘backup’ pacemakers (if SA node fails) or pathological ‘override’ mechanisms (even if SA node is functional).
15
Q
Why might a rhythm arise from a site other than the SA node?
A
Either due to SA node failure or abnormal overriding mechanisms.
16
Q
What are ‘back-up’ pacemakers?
A
Pacemaker cells outside the SA node that take over if the SA node fails.
17
Q
Why are back-up pacemakers normally suppressed?
A
SA node depolarization suppresses them under normal conditions.
18
Q
What happens when the SA node fails?
A
Back-up pacemakers are free to depolarize and assume the main pacemaker role.
19
Q
How does the rate of back-up pacemakers compare to the SA node?
A
They are slower than the SA node, ranging from slow-normal to bradycardia.
20
Q
Are back-up pacemaker rhythms regular or irregular?
A
Regular, because their depolarization occurs in consistent cycles.
21
Q
How does the QRS width of a back-up pacemaker beat vary?
A
It depends on the pacemaker’s location in the heart.
22
Q
Can back-up pacemakers cause tachycardia?
A
No. They may accelerate via sympathetic stimulation but will not produce tachycardia
23
Q
Why are back-up pacemakers important?
A
They are lifesaving, ensuring the heart continues to beat if the SA node fails.
24
Q
What are “override mechanisms” in cardiac electrophysiology?
A
They are mechanisms where impulses other than the SA node suppress its normal pacemaking function, either through ectopic pacemakers or reentry circuits, potentially causing tachycardia.
25
What is an ectopic pacemaker?
A myocardial cell that develops abnormal automaticity and can generate impulses that override the SA node, such as in ventricular tachycardia (VT).
26
How do reentry circuits cause override of the SA node?
They occur when impulses loop repeatedly through a pathway, either due to chronic tissue changes (e.g., atrial flutter) or congenital pathways (e.g., WPW), bypassing normal SA node control.
27
What heart rate is typically associated with override mechanisms?
Tachycardias faster than 120 beats per minute (b/m).
28
How does the AV node affect supraventricular tachyarrhythmias?
The parasympathetic AV node can block conduction from ectopic pacemakers or reentry circuits proximally, resulting in a fast atrial rate but a normal or slow ventricular (QRS) rate.
29
Give an example of a condition where the AV node moderates tachycardia.
Atrial flutter often shows a fast atrial rate but a normal or slow QRS rate due to AV nodal conduction control.
30
Why should rhythm abnormalities be approached with caution?
Because the autonomic nervous system can create “grey areas” and exceptions, moderating the ventricular response and making tachycardias or bradycardias less predictable.
31
What is the simple general rule when approaching brady-arrhythmias on ECG?
Look for the relationship between P-waves and QRS complexes to decide whether the problem is sinus rhythm, conduction, or impulse formation
32
If each P-wave is followed by a QRS complex, what is the diagnosis?
Sinus bradycardia.
33
If QRS complexes are missing, what is the cause of the slow heart rate?
Abnormal conduction of impulses.
34
If P-waves are missing, what is the cause of the slow heart rate?
Abnormal formation of impulses.
35
What is a junctional rhythm?
A rhythm arising from a back-up pacemaker in the AV node when the SA node fails to depolarize.
36
Why does a junctional rhythm occur?
Because the SA node fails, allowing the AV nodal pacemaker to drift into depolarization and assume control.
37
What is the typical heart rate in a junctional rhythm?
40–60 beats per minute.
38
Is a junctional rhythm regular or irregular?
Regular
39
What is the QRS duration in a junctional rhythm?
Narrow QRS (<120 ms).
40
Why is the QRS narrow in junctional rhythms?
Because ventricular depolarization occurs via the normal, fast His–Purkinje “highway.”
41
What happens to atrial depolarization in a junctional rhythm?
A retrograde P-wave spreads from the AV node back through the atria in the opposite direction to normal.
42
How does the retrograde direction affect the P-wave in lead II?
The P-wave is inverted (negative) in lead II.
43
How does the P-wave appear in lead aVR during a junctional rhythm?
Upright (positive).
44
Why may P-waves be absent in a junctional rhythm?
They may be hidden within the QRS complex due to simultaneous atrial and ventricular depolarization.
45
What are the three possible P-wave positions in a junctional rhythm?
* Hidden within the QRS
* Before the QRS (inverted in lead II)
* Immediately after the QRS as an inverted “notch”
46
Are P-waves, when visible, linked to the QRS in junctional rhythms?
Yes, P-waves are connected to the QRS complex.
47
When do ventricular rhythms usually occur?
Most commonly in complete (3rd degree) heart block at the AV node or Bundle of His, preventing supraventricular impulses from reaching the ventricles.
48
Why does a ventricular pacemaker take over in complete heart block?
Because the ventricles are electrically isolated from atrial impulses, allowing a ventricular pacemaker to slowly drift into depolarization.
49
Where do most ventricular pacemakers originate?
In the left or right ventricle.
50
What is the typical rate of a ventricular pacemaker rhythm?
Very slow: 15–40 beats per minute.
51
Is the ventricular pacemaker rhythm regular or irregular?
Regular
52
What is the QRS duration in ventricular pacemaker rhythms?
Wide QRS (>120 ms).
53
What is the relationship between P-waves and QRS complexes in ventricular rhythms?
P-waves are NOT connected to QRS complexes, and there are usually more P-waves than QRS complexes.
54
Why is the QRS wide in ventricular pacemaker rhythms?
Because depolarization spreads slowly through ventricular myocardium instead of the fast His–Purkinje system.
55
How does the QRS complex typically appear in ventricular rhythms?
Bizarre and often notched.
56
What is the typical T-wave appearance in ventricular pacemaker rhythms?
The T-wave is in the opposite direction to the QRS complex.
57
Where does a high or infranodal pacemaker arise?
In the Bundle of His.
58
How common are infranodal pacemakers compared to ventricular pacemakers?
Less common.
59
What is the typical rate of an infranodal pacemaker rhythm?
40–60 beats per minute.
60
What is the QRS width in infranodal pacemaker rhythms?
Borderline or near-normal width.
61
What is the relationship between P-waves and QRS complexes in infranodal rhythms?
P-waves are NOT connected to QRS complexes, with more P-waves than QRS complexes.
62
How does the QRS morphology differ from ventricular pacemaker rhythms?
The QRS looks normal and is not bizarre.
63
What happens to the T-wave in infranodal pacemaker rhythms?
The T-wave is not affected.
64
Why can 3rd-degree AV block with a ventricular pacemaker be difficult to diagnose?
Because both P-waves and QRS complexes are present, but they occur independently of each other.
65
66
What is the most important first step when suspecting a 3rd-degree AV block?
Identify the P-waves first.
67
What characteristics must P-waves have to confirm they are true P-waves?
They must look like P-waves and be regular.
68
After identifying P-waves, what is the next step in ECG analysis?
Identify the QRS complexes and assess their relationship to the P-waves.
69
What should be assessed when comparing P-waves and QRS complexes?
Whether the P-waves and QRS complexes are connected.
70
What does a constant PR relationship indicate?
Normal AV conduction or a fixed-ratio block, not 3rd-degree block.
71
What finding strongly suggests a 3rd-degree AV block?
P-waves vary in their relationship to the QRS complexes or appear randomly before, within, or after the QRS.
72
What is the key ECG hallmark of 3rd-degree AV block?
Complete AV dissociation between atrial and ventricular activity.
73
Why are there usually more P-waves than QRS complexes in 3rd-degree block?
Because the atria and ventricles are depolarizing independently.
74
What rhythm should be suspected when P-waves are regular but unrelated to a slow, wide QRS rhythm?
3rd-degree AV block with a ventricular pacemaker.
75
How may tachyarrhythmias be preceded clinically or on ECG?
By “warning salvos” of ectopic beats appearing as extra, premature waves on the underlying rhythm.
76
What is an ectopic beat?
A premature depolarization arising from a focus outside the SA node.
77
Why are ectopic beats described as premature?
Because they occur earlier than expected in the normal cardiac cycle.
78
Why are ectopic beats important in the approach to tachy-arrhythmias?
They may act as triggers for sustained tachyarrhythmias.
79
Where do premature atrial contractions (PACs) originate?
From an ectopic focus in the atria.
80
What is the QRS width in PACs?
Narrow QRS complexes.
81
Why is the QRS narrow in PACs?
Because ventricular depolarization occurs via the normal His–Purkinje system.
82
How does the R–R interval appear before a PAC?
It is shortened because the beat occurs prematurely.
83
Are PACs usually followed by a pause?
No, they are usually followed by an incomplete pause
84
Why do PACs cause an incomplete pause rather than a full compensatory pause?
Because the abnormal atrial beat generates a retrograde wave that resets the timing of SA node depolarization
85
What does “resetting of the SA node” mean?
The ectopic atrial impulse alters the normal timing of the next SA node discharge.
86
How can PACs be distinguished from ventricular ectopic beats on ECG?
PACs have narrow QRS complexes, whereas ventricular ectopic beats have wide, bizarre QRS complexes
87
What is a premature ventricular contraction (PVC)?
A premature ectopic beat originating in the ventricles.
88
What is the QRS appearance in a PVC?
Wide and abnormally shaped (bizarre) QRS complexes
89
Is a P-wave present before a PVC?
No, PVCs occur without a preceding P-wave.
90
What happens to the R–R interval before a PVC?
It is shortened because the beat occurs prematurely.
91
What happens to the R–R interval after a PVC?
It appears prolonged, often twice the usual R–R interval (a full compensatory pause).
92
Why does a pause occur after a PVC?
Because the ventricles remain refractory from the abnormal depolarization, blocking the next SA-node impulse from being conducted below the AV node.
93
Is the SA node reset by a PVC?
No, the SA node is not reset.
94
Why is the SA node not reset in PVCs?
Because ventricular impulses cannot spread retrograde to the atria.
95
What key feature distinguishes PVCs from PACs regarding pauses?
PVCs are followed by a full compensatory pause, while PACs are followed by an incomplete pause.
96
What ECG clues strongly suggest a PVC?
Wide bizarre QRS, no preceding P-wave, premature beat, and a full compensatory pause afterward.
97
What is a premature complex?
An ectopic beat that occurs earlier than expected, interrupting an underlying rhythm.
98
What is a physiological (escape) pacemaker?
A back-up pacemaker that fires because the primary pacemaker (SA node) fails or slows.
99
When does a premature complex occur in the cardiac cycle?
Early (prematurely), before the next expected SA node beat
100
When does a physiological pacemaker fire?
Late, after a pause when the SA node fails to depolarize on time.
101
Why do premature complexes occur?
Due to abnormal automaticity or triggered activity from an ectopic focus.
102
Why do physiological pacemakers occur?
Because of sinus node failure, sinus pause, or high-grade AV block.
103
Does a premature atrial complex reset the SA node?
Yes, PACs reset the SA node via retrograde conduction
104
Does a premature ventricular complex reset the SA node?
No, PVCs cannot conduct retrograde to the atria.
105
Do physiological pacemakers reset the SA node?
No, they activate only because the SA node has failed to fire.
106
What type of pause follows a PAC?
An incomplete pause.
107
What type of pause follows a PVC?
A full compensatory pause.
108
Is there a pause after a physiological pacemaker beat?
No compensatory pause — the beat occurs late, not early.
109
How does a premature complex appear on ECG in relation to timing?
As an early beat with a shortened preceding R–R interval.
110
How does a physiological pacemaker beat appear on ECG?
As a delayed beat occurring after a pause
111
In what rate context do premature complexes usually occur?
Normal or fast underlying rhythms.
112
In what rate context do physiological pacemakers usually occur?
Slow rhythms (bradycardia).
113
What is the single most important ECG clue to distinguish the two?
premature complexes vs physiological pacemakers
Timing: premature complexes are early; physiological pacemakers are late.
114
Why is this distinction clinically important of premature complexes vs physiological pacemakers
Premature complexes may trigger tachyarrhythmias, while physiological pacemakers are protective escape mechanisms.
115
What happens when extra beats increase in frequency?
They may suppress and take over the pacemaking function of the SA node.
116
Besides frequent ectopic beats, what other mechanism can suppress the SA node?
Activation of a reentry circuit.
117
Why does suppression of the SA node lead to tachyarrhythmias?
Because ectopic pacemakers or reentry circuits fire faster than the SA node.
118
When does a tachyarrhythmia produce a regular rhythm?
When it arises from a single ectopic focus or a single reentry pathway.
119
When does a tachyarrhythmia produce an irregular rhythm?
When it arises from multiple ectopic sites or multiple reentry circuits.
120
What determines the width of the QRS complex in tachyarrhythmias?
Whether the origin of the rhythm is supraventricular or ventricular.
121
Why are supraventricular tachyarrhythmias usually narrow-complex?
Because ventricular depolarization occurs via the normal His–Purkinje system.
122
Why are ventricular tachyarrhythmias usually wide-complex?
Because depolarization spreads slowly through ventricular myocardium.
123
What is atrial tachycardia (AT)?
A sustained tachyarrhythmia caused by an ectopic pacemaker arising from a single site in the atria.
124
Is atrial tachycardia regular or irregular?
Regular
125
Why is atrial tachycardia considered a sustained ectopic rhythm?
Because one atrial ectopic focus continuously overrides the SA node.
126
What is the expected QRS width in atrial tachycardia?
Narrow QRS complexes (unless there is aberrant conduction).
127
How does the SA node behave during atrial tachycardia?
It is suppressed by the faster ectopic atrial pacemaker.
128
What is the key ECG hallmark of atrial tachycardia?
A single abnormal P-wave morphology.
129
Why is the P-wave abnormal in atrial tachycardia?
Because atrial depolarization originates from an ectopic atrial focus rather than the SA node.
130
Is the rhythm in atrial tachycardia regular or irregular?
Regular
131
What happens to the heart rate in atrial tachycardia?
It is fast (tachycardia).
132
What is the QRS width in atrial tachycardia?
Narrow QRS complexes.
133
Why is the QRS narrow in atrial tachycardia?
Ventricular depolarization occurs through the normal His–Purkinje conduction system
134
How does atrial tachycardia suppress the SA node?
The faster ectopic atrial pacemaker overrides normal SA node depolarization.
135
What ECG finding helps distinguish atrial tachycardia from sinus tachycardia?
A P-wave shape that is different from the normal sinus P-wave.
136
What is multifocal atrial tachycardia (MAT)?
A tachyarrhythmia caused by multiple sustained ectopic pacemakers in the atria.
137
From where do impulses originate in MAT?
From multiple sites within the atria.
138
What is the key ECG feature of the P-waves in MAT?
Several abnormal P-wave morphologies.
139
Why are P-waves different in shape in MAT?
Because atrial depolarization arises from multiple ectopic atrial foci.
140
Is every QRS complex preceded by a P-wave in MAT?
Yes, every QRS is preceded by a P-wave.
141
Is the rhythm in MAT regular or irregular?
Irregular
142
What happens to the heart rate in MAT?
It is fast (tachycardia).
143
What is the QRS width in MAT?
Narrow QRS complexes.
144
Why is the QRS narrow in MAT?
Ventricular depolarization occurs via the normal His–Purkinje system.
145
What ECG finding distinguishes MAT from atrial tachycardia?
MAT has multiple abnormal P-wave shapes, whereas atrial tachycardia has a single abnormal P-wave shape.
146
What ECG finding helps distinguish MAT from atrial fibrillation?
MAT has visible P-waves before every QRS, while atrial fibrillation has no discrete P-waves.
147
What is atrial flutter?
A supraventricular tachyarrhythmia caused by a reentry circuit, usually circulating around the right atrium.
148
How fast does the atrial depolarization occur in atrial flutter?
Approximately every 0.2 seconds, producing about 250–350 atrial beats per minute (often ~300 bpm).
149
What produces the characteristic “flutter waves” in atrial flutter?
Rapid, repetitive atrial depolarization from the reentry circuit.
150
Why does the AV node not conduct every flutter wave to the ventricles?
Because it cannot manage such high atrial depolarization rates.
151
What is the most common AV conduction ratio in atrial flutter?
2:1 block.
152
What ventricular rate results from a 2:1 block in atrial flutter?
150 beats per minute.
153
What ventricular rates are seen with other AV block ratios in atrial flutter?
* 3:1 → 100 bpm
* 4:1 → 75 bpm
* 5:1 → 60 bpm
154
What determines the degree of AV block in atrial flutter?
The amount of parasympathetic (vagal) action exerted on the AV node.
155
Why can atrial flutter be difficult to recognize on ECG?
Because flutter waves may be hidden within QRS complexes at fast conduction ratios.
156
How can vagal maneuvers help diagnose atrial flutter?
by increasing AV nodal block, which uncovers the underlying flutter waves.
157
What are the typical ventricular rates seen in atrial flutter?
150, 100, 75, or 60 beats per minute.
158
What is the QRS appearance in atrial flutter?
Narrow QRS complexes.
159
Are P-waves easy to identify in atrial flutter?
No, P-waves are often difficult to identify when conduction is fast.
160
What is the classic ECG appearance of atrial flutter waves?
Saw-tooth shaped flutter waves.
161
In which ECG lead are flutter waves most clearly seen?
Lead II.
162
What is atrial fibrillation (AF)?
A supraventricular arrhythmia caused by multiple reentry circuits producing chaotic atrial depolarization.
163
How fast do atrial impulses occur in atrial fibrillation?
More than 300 impulses per minute.
164
More than 300 impulses per minute.
Small, chaotic depolarization waves generated by multiple reentry circuits in the atria.
165
Why is the ventricular rhythm irregular in atrial fibrillation?
Because the AV node allows only some atrial impulses to pass through in an unpredictable manner.
166
What types of ventricular rates can be seen in atrial fibrillation?
Fast, normal, or slow
167
What is the typical QRS width in atrial fibrillation?
Narrow QRS complexes.
168
When might the QRS be wide in atrial fibrillation?
In the presence of pre-existing conditions such as bundle branch block (BBB).
169
Are normal P-waves present in atrial fibrillation?
No, there are no discernible P-waves.
170
What replaces P-waves on the ECG in atrial fibrillation?
Irregular fibrillatory wavelets appearing as “squiggly” baseline activity.
171
Is there a repeating pattern to the baseline in atrial fibrillation?
No, the baseline has no discernible pattern.
172
How is the rhythm described in atrial fibrillation?
Irregularly irregular.
173
What is the single most important ECG clue to atrial fibrillation?
An irregularly irregular rhythm with no identifiable P-waves
174
Can ectopic beats occur on top of atrial fibrillation?
Yes, ectopic beats such as PVCs may be superimposed on the baseline.
175
What is a couplet in atrial fibrillation?
Two consecutive premature ventricular contractions occurring together.
176
What is AV nodal re-entry tachycardia (AVNRT)?
A supraventricular tachycardia caused by a reentry circuit within the AV node.
177
What anatomical abnormality allows AVNRT to occur?
The presence of two excitation pathways within the AV node.
178
How do the two AV nodal pathways differ?
They have different conduction velocities.
179
What are the two AV nodal pathways commonly called?
A fast pathway and a slow pathway.
180
What happens during normal conduction in a patient with dual AV nodal pathways?
The impulse travels down the fast pathway and dies out in the slow pathway.
181
Why does tachycardia not occur during normal conduction?
Because the impulse cannot complete a reentry circuit
182
What event commonly triggers AVNRT?
A premature atrial beat.
183
What happens if a premature beat occurs while the fast pathway is still refractory?
The impulse is forced to conduct down the slow pathway.
184
What occurs by the time the impulse reaches the distal AV node via the slow pathway?
The fast pathway has repolarized.
185
What does this allow the impulse to do in AVRNT
Conduct retrogradely up the fast pathway.
186
What is formed when the impulse travels down the slow pathway and up the fast pathway?
A reentry circuit or loop.
187
What is the clinical consequence of this reentry circuit?
Sustained tachycardia.
188
Why is refractoriness critical in the development of AVNRT?
Because differential refractoriness allows unidirectional conduction and reentry.
188
189
Where is the reentry circuit located in AVNRT?
Within the AV node itself.
190
Why are P-waves difficult to identify in AVNRT?
Because the ventricular rate is very fast, causing P-waves to be hidden within or immediately after the QRS complexes.
191
In which patients should AVNRT be strongly suspected?
Young patients presenting with a very fast supraventricular tachycardia.
192
What heart rate is typical of AVNRT
Greater than 200 beats per minute.
193
What is the rhythm regularity in AVNRT?
Regular.
194
What is the QRS width in AVNRT?
Narrow QRS complexes.
195
What ECG pattern strongly suggests AVNRT in a beginner-level assessment?
A very fast (>200 bpm), regular, narrow-complex tachycardia with no clearly visible P-waves.
196
Why does AVNRT respond well to vagal maneuvers?
Because the reentry circuit involves the AV node.
197
What effect do vagal maneuvers have on the AV node?
They increase parasympathetic tone, slowing AV nodal conduction.
198
What is the effect of vagal maneuvers on AVNRT?
Termination of the tachycardia.
199
What is the most likely diagnosis in a young patient with a very fast, regular, narrow-complex tachycardia?
AV nodal re-entry tachycardia (AVNRT).
200
What is ventricular tachycardia (VT)?
A tachyarrhythmia originating in the ventricles, due to either an ectopic focus or a reentry circuit.
201
What heart rate range is typical of VT?
Greater than 120 beats per minute.
202
Why is VT the default diagnosis in fast, wide-complex tachycardias?
For reasons of safety and probability — VT is the most common and most dangerous cause.
203
How common is VT compared to other wide-complex tachycardias?
How common is VT compared to other wide-complex tachycardias?
204
What is the typical rhythm regularity in VT?
Regular
205
What is the QRS width in VT?
Wide QRS complexes (>120 ms).
206
How do the QRS complexes appear in monomorphic VT?
Wide, bizarre, and identical in shape from beat to beat.
207
Do VT QRS complexes usually resemble typical bundle branch block patterns?
No, they do not have a typical bundle branch block morphology.
208
Are P-waves usually visible in VT?
No, P-waves are seldom visible
209
What is monomorphic ventricular tachycardia?
VT in which all QRS complexes have the same shape and axis.
210
What does monomorphic VT suggest about the mechanism?
A single ectopic focus or a single reentry circuit in the ventricles.
211
What are the possible outcomes of VT?
* Self-termination
* Sustained VT
* Degeneration into ventricular fibrillation (VF)
212
Why is VT considered a life-threatening arrhythmia?
Because it can rapidly compromise cardiac output or deteriorate into VF.
213
How should a fast, regular, wide-complex rhythm be approached initially?
Assume ventricular tachycardia until proven otherwise.
214
What ECG combination most strongly suggests VT?
Fast rate, regular rhythm, wide identical QRS complexes, and absent or dissociated P-waves.
215
Why is misdiagnosing VT as SVT with aberrancy dangerous?
Because treating VT as SVT may delay life-saving therapy and worsen outcomes.
216
What is the default diagnosis in a fast, regular, wide-QRS tachycardia?
Ventricular tachycardia (VT), for safety and probability
217
When is it acceptable to diagnose supraventricular tachycardia (SVT) instead of VT?
Only when a definite bundle branch block (BBB) pattern can be clearly identified
218
What ECG feature confirms left bundle branch block (LBBB)?
An M-shaped QRS complex in lead V6.
219
What ECG feature confirms right bundle branch block (RBBB)?
An RSR′ pattern in lead V1.
220
Why must the BBB pattern be distinct to diagnose SVT with aberrancy?
Because vague or atypical wide QRS morphologies are more likely due to VT.
221
How should a fast, regular, wide-complex rhythm be labeled if BBB morphology is unclear?
Ventricular tachycardia until proven otherwise.
222
What does a typical BBB pattern suggest in a tachycardia?
A supraventricular rhythm conducting abnormally through the ventricles (SVT + BBB).
223
Why is this rule emphasized in beginners?
Because mislabeling VT as SVT can lead to dangerous management errors.
224
Complete this rule: “Fast + regular + wide QRS = ____ unless proven otherwise.”
Ventricular tachycardia.
225
What is polymorphic ventricular tachycardia (P-VT)?
A ventricular tachycardia in which the QRS complexes vary in shape and axis beat-to-beat.
226
How does P-VT differ clinically from ventricular fibrillation (Vfib)?
P-VT still has a palpable (weak, irregular) pulse, whereas Vfib has no pulse.
227
Why can P-VT be confused with coarse Vfib?
Because both show chaotic, irregular ventricular activity with changing amplitudes.
228
What is torsades de pointes?
A specific form of polymorphic VT associated with a prolonged QT interval.
229
Why can the QT interval usually not be measured during torsades?
The rhythm is too fast and unstable to identify clear QT boundaries.
230
How is torsades de pointes diagnosed on ECG?
By its characteristic undulating, twisting QRS complexes around the baseline.
231
What does the name “torsades de pointes” mean?
“Twisting of the points,” describing the rotating QRS morphology.
232
Why is polymorphic VT considered an emergency?
It is haemodynamically unstable and may degenerate into ventricular fibrillation.
233
What is the major life-threatening complication of P-VT
Sudden deterioration into Vfib and cardiac arrest.
234
A patient has a fast, chaotic wide-complex rhythm with a weak pulse—what is the diagnosis?
Polymorphic ventricular tachycardia, not Vfib.
235
What is Ventricular Fibrillation (Vfib)?
Vfib is a life-threatening arrhythmia where the ventricles quiver chaotically instead of contracting effectively, resulting in no cardiac output.
236
How does Vfib appear on an ECG?
The ECG shows rapid, irregular, and chaotic ventricular activity without identifiable P waves, QRS complexes, or T waves. It can be coarse or fine.
237
What is the difference between coarse and fine Vfib?
- Coarse Vfib: Larger, more visible fibrillatory waves; easier to recognize on ECG.
Fine Vfib: Smaller, subtle waves; may be mistaken for asystole.
238
Why can fine Vfib be confused with asystole?
Because the amplitude of the ventricular waves is very low, making the ECG appear almost flat, similar to asystole.
239
What are the clinical signs of Vfib?
Sudden collapse, loss of consciousness, absence of pulse, and no effective breathing. It is immediately life-threatening.
240
What is the first-line treatment for Vfib?
Immediate defibrillation (unsynchronized shock) and CPR until defibrillation is available.
241
Which medications may be used during Vfib management?
- Epinephrine (adrenaline)
Amiodarone (antiarrhythmic) if Vfib persists after defibrillation
242
What are common causes of Vfib?
- Myocardial infarction
Severe electrolyte disturbances (e.g., hyperkalemia, hypokalemia)
Cardiomyopathy
Drug toxicity (e.g., antiarrhythmics, digoxin)
Hypoxia
General Medicine
flashcards
Decks in class (37)
# Cards
-
EOB Exams659
-
ECG Module 196
-
ECG Module 2153
-
ECG Module 3: normal sinus rhythm284
-
ECG Module 4: Wave abnormalities324
-
ECG Module 5: Rhythm abnormalities243
-
Chest X- ray165
-
Hypertension52
-
Advanced Airway Management341
-
CPR48
-
Post Cardiac Arrest Care35
-
CardioPulmonary Resuscitation532
-
Basic Airway Management122
-
Capnography41
-
Ventilator Settings27
-
Ventilation15
-
Anaphylaxis130
-
Cardiac Infections75
-
Benzodiazepine Overdose112
-
Iron Overdose92
-
Opioid Overdose122
-
Paracetamol Overdose107
-
TCA Overdose80
-
Bradycardia198
-
Tachycardia251
-
Hyponatremia121
-
Hyperthermia27
-
Hypothermia71
-
Hypertensive Emergency146
-
Delirium127
-
Sepsis105
-
Status Epilepticus108
-
Snack bites155
-
Acute Kidney Injury101
-
Pneumonia22
-
Bronchiectasis23
-
COPD40
